Optimal suppression of thromboxane A(2) formation by aspirin during percutaneous transluminal coronary angioplasty: no additional effect of a selective cyclooxygenase-2 inhibitor.
D015906:Angioplasty, Balloon, Coronary; D001241:Aspirin / Q000627:therapeutic use*; D001713:Biphenyl Compounds / Q000627:therapeutic use*; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; D015237:Dinoprost / Q000031:analogs & derivatives* / Q000096:biosynthesis* / Q000652:urine; D011464:Epoprostenol / Q000502:physiology*; D005260:Female; D006801:Humans; D007527:Isoenzymes / Q000037:antagonists & inhibitors* / Q000502:physiology; D008297:Male; D008565:Membrane Proteins; D008875:Middle Aged; D010544:Peroxidases / Q000037:antagonists & inhibitors; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors; D011451:Prostaglandin-Endoperoxide Synthases / Q000502:physiology; D011759:Pyrrolidines / Q000627:therapeutic use*; D013449:Sulfonamides / Q000627:therapeutic use*; D013928:Thromboxane A2 / Q000096:biosynthesis* / Q000652:urine
D001713:Biphenyl Compounds; D007527:Isoenzymes; D008565:Membrane Proteins; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D011759:Pyrrolidines; D013449:Sulfonamides; C075750:8-epi-prostaglandin F2alpha; D013928:Thromboxane A2; D015237:Dinoprost; D011464:Epoprostenol; C107917:fradafiban; D010544:Peroxidases; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; C496511:PTGS1 protein, human; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases; D001241:Aspirin; C012655:nimesulide